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Sagar U. Nigwekar, Ishir Bhan, Ravi Thadhani, Nutritional vitamin D in dialysis patients: what to D-iscern?, Nephrology Dialysis Transplantation, Volume 26, Issue 3, March 2011, Pages 764–766, https://doi.org/10.1093/ndt/gfq799
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Worldwide, ∼2 million patients rely on chronic dialysis therapy to sustain their life [1,2]. Despite advances in therapies and technology, mortality and morbidity in the dialysis population remain high. Cardiovascular disease is the leading cause of mortality in this population [3] and the search remains active for ‘modifiable factors’ that will improve outcomes in this patient population.
Vitamin D, traditionally thought to be involved only in bone and mineral metabolism, has been increasingly reported to have significant extraskeletal actions [4,5]. These include its effects on monocyte–macrophages (expression of the cathelicidin antimicrobial peptide), lymphocytes (cytokine release), pancreas (insulin production) and kidney (renin production). Studies have suggested that vitamin D has anticancer properties through its effects on cellular proliferation, differentiation, apoptosis and angiogenesis. It has been shown to be involved in the growth and proliferation of vascular smooth muscle cells and cardiomyocytes [4,6]. Vitamin D traditionally exerts its effects on bone and mineral metabolism in its hormone form, 1,25-dihydroxyvitamin D (1,25-D). In patients with normal renal function, inadequate supply of substrate 25-hydroxyvitamin D (25-D) will stimulate the 1-α hydroxylase enzyme in proximal renal tubular cells to maintain levels of 1,25-D, an effect mediated via an increase in parathyroid hormone (PTH) production; fibroblast growth factor 23 (FGF-23) acts as a counter-regulatory hormone, suppressing 1-α hydroxylase and reducing conversion of 25-D to 1,25-D [7]. In contrast to the endocrine effects of vitamin D on bone mineral metabolism, its extraskeletal effects are exerted as paracrine and autocrine actions; local production at sites of action may be essential. Reduced delivery of 25-D to target tissues will result in reduced intracellular conversion to 1,25-D independent of renal 1-α hydroxylase activity.
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